Expert Opinion on Therapeutic Targets最新文献_第2页

IF 4.6 2区医学

Expert Opinion on Therapeutic Targets Pub Date : 2025-04-01 Epub Date: 2025-05-12 DOI: 10.1080/14728222.2025.2500422

Marian Vincenzi, Flavia Anna Mercurio, Marilisa Leone

{"title":"Cataract-related mutations in EphA2: a survey of literature data and the relevance of the receptor Sam domain.","authors":"Marian Vincenzi, Flavia Anna Mercurio, Marilisa Leone","doi":"10.1080/14728222.2025.2500422","DOIUrl":"https://doi.org/10.1080/14728222.2025.2500422","url":null,"abstract":"Introduction: EphA2 is a receptor tyrosine kinase that is associated with various pathological conditions. Mutations in EphA2 are linked to cataract, an eye disorder manifesting as lens opacity, and representing one of the most prominent causes of blindness worldwide.Areas covered: We collected a list of cataract-related EphA2 mutations and positioned them inside the different protein domains to identify regions of the receptor that could be more likely considered targets in the 'anti-cataract' drug discovery field. Moreover, we analyzed the structural consequences these mutations could induce. A search for literature related to EphA2 and cataracts was carried out through the PubMed National Library of Medicine. Structural information on diverse EphA2 domains was obtained from the Protein Data Bank. EphA2 variants connected to cataract were checked on the databases Cat-Map and dbSNP.Expert opinion: Cataract-related mutations are gathered within diverse EphA2 domains and are abundant inside its Sam (Sterile alpha motif, EphA2-Sam) domain. Mutations affecting EphA2-Sam could disturb domain helical fold and hamper interaction with other Sam domains, eventually interfering with EphA2 cell migration activity. Identification of stabilizing small molecules targeting EphA2-Sam pathogenic variants could represent an original route to discover novel therapeutic compounds against lens opacity.","PeriodicalId":12185,"journal":{"name":"Expert Opinion on Therapeutic Targets","volume":"29 4-5","pages":"239-265"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Restoring FXR expression as a novel treatment strategy in liver cancer and other liver disorders. 恢复FXR表达作为肝癌和其他肝脏疾病的新治疗策略。

IF 4.6 2区医学

Expert Opinion on Therapeutic Targets Pub Date : 2025-04-01 Epub Date: 2025-05-11 DOI: 10.1080/14728222.2025.2487465

Sosmitha Girisa, Babu Santha Aswani, Mukesh Kumar Manickasamy, Mangala Hegde, Mohammed S Alqahtani, Mohamed Abbas, Gautam Sethi, Ajaikumar B Kunnumakkara

{"title":"Restoring FXR expression as a novel treatment strategy in liver cancer and other liver disorders.","authors":"Sosmitha Girisa, Babu Santha Aswani, Mukesh Kumar Manickasamy, Mangala Hegde, Mohammed S Alqahtani, Mohamed Abbas, Gautam Sethi, Ajaikumar B Kunnumakkara","doi":"10.1080/14728222.2025.2487465","DOIUrl":"10.1080/14728222.2025.2487465","url":null,"abstract":"Introduction: Liver cancer is a leading cause of cancer-associated mortality and is often linked to preexisting liver conditions. Emerging research demonstrates FXR dysregulation, particularly its reduced expression, in the pathogenesis of liver diseases, including inflammation, fibrosis, cholestatic disorders, metabolic dysregulation, and liver cancer. Therefore, this review explores the role of FXR and its agonists in mitigating these conditions.Areas covered: This article summarizes FXR's involvement in liver disorders, primarily emphasizing on hepatic neoplasms, and examines the potential of FXR agonists in restoring FXR activity in liver diseases, thereby preventing their progression to liver cancer. The information presented is drawn from existing preclinical and clinical studies specific to each liver disorder, sourced from PubMed.Expert opinion: It is well established that FXR expression is downregulated in liver disorders, contributing to disease progression. Notably, FXR agonists have demonstrated therapeutic potential in ameliorating liver diseases, including hepatocellular carcinoma. We believe that activating or restoring FXR expression with agonists offers significant promise for the treatment of liver cancer and other liver conditions. Therefore, FXR modulation by agonists, particularly in combination with other therapeutic agents, could lead to more targeted treatments, improving efficacy while reducing side effects.","PeriodicalId":12185,"journal":{"name":"Expert Opinion on Therapeutic Targets","volume":" ","pages":"193-221"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LPAR5 as a prospective therapeutic target for treating microvillus inclusion disease. LPAR5作为治疗微绒毛包涵性疾病的前瞻性治疗靶点。

IF 4.6 2区医学

Expert Opinion on Therapeutic Targets Pub Date : 2025-04-01 Epub Date: 2025-05-02 DOI: 10.1080/14728222.2025.2500416

Andreanna Burman, Izumi Kaji

引用次数: 0

Preclinical targeting of leukemia-initiating cells in the development future biologics for acute myeloid leukemia. 白血病起始细胞在急性髓性白血病生物制剂开发中的临床前靶向作用。

IF 4.6 2区医学

Expert Opinion on Therapeutic Targets Pub Date : 2025-04-01 Epub Date: 2025-05-06 DOI: 10.1080/14728222.2025.2500417

Jiaxin Dong, Marina Konopleva

{"title":"Preclinical targeting of leukemia-initiating cells in the development future biologics for acute myeloid leukemia.","authors":"Jiaxin Dong, Marina Konopleva","doi":"10.1080/14728222.2025.2500417","DOIUrl":"https://doi.org/10.1080/14728222.2025.2500417","url":null,"abstract":"Introduction: Leukemia-initiating cells (LICs) are a critical subset of cells driving acute myeloid leukemia (AML) relapse and resistance to therapy. They possess unique properties, including metabolic, epigenetic, and microenvironmental dependencies, making them promising therapeutic targets.Areas covered: This review summarizes preclinical advances in targeting AML LICs, including strategies to exploit metabolic vulnerabilities, such as the reliance on oxidative phosphorylation (OXPHOS), through the use of mitochondrial inhibitors; target epigenetic regulators like DOT1L (Disruptor of Telomeric Silencing 1-like) to disrupt LIC survival mechanisms; develop immunotherapies, including CAR (chimeric antigen receptor) T-cell therapy, and bispecific antibodies; and disrupt LIC interactions with the bone marrow microenvironment by inhibiting supportive niches.Expert opinion: LIC-targeted therapies hold significant promise for revolutionizing AML treatment by reducing relapse rates and improving long-term outcomes. However, challenges such as LIC heterogeneity, therapy resistance, and associated toxicity persist. Recent studies have illuminated the distinct biological characteristics of LICs, advancing our understanding of their behavior and vulnerabilities. These insights offer new opportunities to target LICs at earlier disease stages and to explore combination therapies with other targeted treatments, ultimately enhancing therapeutic efficacy and improving patient outcomes.","PeriodicalId":12185,"journal":{"name":"Expert Opinion on Therapeutic Targets","volume":"29 4-5","pages":"223-237"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

NLRP3 inflammasome: significance and potential therapeutic targets to advance solid organ transplantation. NLRP3炎性体：促进实体器官移植的意义和潜在治疗靶点。

IF 4.6 2区医学

Expert Opinion on Therapeutic Targets Pub Date : 2025-04-01 Epub Date: 2025-05-07 DOI: 10.1080/14728222.2025.2500425

Pershia Davoodi Karsalari, Kosar Asna Ashari, Nima Rezaei

{"title":"NLRP3 inflammasome: significance and potential therapeutic targets to advance solid organ transplantation.","authors":"Pershia Davoodi Karsalari, Kosar Asna Ashari, Nima Rezaei","doi":"10.1080/14728222.2025.2500425","DOIUrl":"https://doi.org/10.1080/14728222.2025.2500425","url":null,"abstract":"Introduction: NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) inflammasome, integral to innate immunity, has become a pivotal figure in the inflammatory cascade.Areas covered: This article provides an overview of the NLRP3 inflammasome, reviewing its complicated structure, as well as the diverse signals that trigger its assembly. Furthermore, we explored the intricate relationship between the NLRP3 inflammasome and acute and chronic rejection in solid organ transplantation. Solid organ transplantation stands as a crucial medical intervention, yet its efficacy is challenged by immune-mediated complications, including acute rejection, ischemia-reperfusion injury, and chronic allograft rejection. We also investigated the encouraging potential of immunosuppressive therapies targeting NLRP3 signaling to alleviate inflammatory responses linked to transplantation.Expert opinion: In recent years, the NLRP3 inflammasome has garnered considerable attention owing to its critical functions spanning diverse fields. This study highlights the critical function of the NLRP3 inflammasome and presents insights, offering fresh perspectives on how its modulation might help to improve the outcomes among patients who undergo solid organ transplantations.","PeriodicalId":12185,"journal":{"name":"Expert Opinion on Therapeutic Targets","volume":"29 4-5","pages":"281-301"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Can we develop effective direct or indirect inhibitors of transcription factors? On the clinical evolution of protein degraders for multiple myeloma therapy. 我们能开发有效的转录因子直接或间接抑制剂吗？蛋白降解物治疗多发性骨髓瘤的临床进展。

IF 4.6 2区医学

Expert Opinion on Therapeutic Targets Pub Date : 2025-03-01 Epub Date: 2025-03-28 DOI: 10.1080/14728222.2025.2482557

Rajeshwari Meli, Osman Aksoy, Sonia Vallet, Dea Slade, Klaus Podar

{"title":"Can we develop effective direct or indirect inhibitors of transcription factors? On the clinical evolution of protein degraders for multiple myeloma therapy.","authors":"Rajeshwari Meli, Osman Aksoy, Sonia Vallet, Dea Slade, Klaus Podar","doi":"10.1080/14728222.2025.2482557","DOIUrl":"10.1080/14728222.2025.2482557","url":null,"abstract":"Introduction: Transcription factors (TFs) are master regulators of cellular function and orchestrate diverse signaling pathways and processes. Acting as convergence points of signaling pathways, they integrate extracellular stimuli with intracellular responses to regulate cell functions. Dysregulation of TFs drives tumorigenesis including proliferation, drug resistance, and immune evasion of multiple myeloma (MM), the second most-common hematologic malignancy.Areas covered: The discovery that IMiDs are molecular glue degraders, which reprogram the E3-ligase cereblon (CRBN) to ubiquitinate and degrade IKZF1 and IKZF3, two otherwise un-druggable crucial TFs in MM, gave rise to the widespread interest in proximity-induced protein-degradation as an exciting novel therapeutic strategy. This review summarizes our up-to-date knowledge on the pre/clinical development of IMiD-related, more potent CRBN E3-Ligase Modulatory Drugs (CELMoDs), directed PROteolysis TArgeting Chimeras (PROTACs) and degronomids as well as on promising future avenues in the field of targeted protein-degradation (TPD).Expert opinion: TPD is an emerging field to treat cancer, including MM. CELMoDs are already reshaping the treatment landscape of MM. Preclinical data on PROTACs are promising. Nevertheless, a deeper understanding of TF biology as well as further advancements in screening methodologies and chemoproteomics are crucial to further spur the transformative potential of targeted TF degradation in MM.","PeriodicalId":12185,"journal":{"name":"Expert Opinion on Therapeutic Targets","volume":" ","pages":"101-115"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Can targeting the FGF23-αKlotho signaling system delay phosphate-driven organ damage? 靶向FGF23-αKlotho信号系统能否延缓磷酸盐驱动的器官损伤？

IF 4.6 2区医学

Expert Opinion on Therapeutic Targets Pub Date : 2025-03-01 Epub Date: 2025-03-28 DOI: 10.1080/14728222.2025.2482552

Mohammed S Razzaque, Moosa Mohammadi

{"title":"Can targeting the FGF23-αKlotho signaling system delay phosphate-driven organ damage?","authors":"Mohammed S Razzaque, Moosa Mohammadi","doi":"10.1080/14728222.2025.2482552","DOIUrl":"10.1080/14728222.2025.2482552","url":null,"abstract":"Introduction: Inexorable high serum phosphate levels in chronic kidney disease (CKD) patients deteriorate the functionality of the musculoskeletal, renal, and cardiovascular systems, thereby contributing to increased morbidity and mortality. Higher phosphate balance has also been correlated with increased mortality rates in individuals with normal renal function, independent of other comorbidities. Clinical and epidemiological studies of CKD patients and healthy subjects, alongside evidence of accelerated aging in murine models induced by excessive phosphate loading, indicate that phosphate toxicity is a driver of premature aging and age-related organ damage.Area covered: This article briefly discusses the causes and consequences of phosphate toxicity in the context of organ damage and aging while also elaborating on the therapeutic potential of the fibroblast growth factor 23 (FGF23) hormone signaling system in alleviating phosphate toxicity in patients with normal kidney function and CKD.Expert opinion: Human age-associated disorders may be delayed through dietary programs or pharmacological interventions capable of modulating the activity of FGF23 signaling to reduce the systemic phosphate burden.","PeriodicalId":12185,"journal":{"name":"Expert Opinion on Therapeutic Targets","volume":" ","pages":"93-100"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MDA-9/Syntenin as a therapeutic cancer metastasis target: current molecular and preclinical understanding. MDA-9/Syntenin作为治疗癌症转移的靶点：目前的分子和临床前认识。

IF 4.6 2区医学

Expert Opinion on Therapeutic Targets Pub Date : 2025-03-01 Epub Date: 2025-03-09 DOI: 10.1080/14728222.2025.2472042

Swadesh K Das, Paul B Fisher

{"title":"MDA-9/Syntenin as a therapeutic cancer metastasis target: current molecular and preclinical understanding.","authors":"Swadesh K Das, Paul B Fisher","doi":"10.1080/14728222.2025.2472042","DOIUrl":"10.1080/14728222.2025.2472042","url":null,"abstract":"Introduction: Metastasis is a principal cause of patient morbidity and death from solid cancers with current therapies being inadequate.Areas covered: Detailed genomic analyses document mutational differences between the initial tumor and metastatic clones, posing a challenge to current targeted therapies, which focus predominantly on the phenotype of primary tumors. Considering the diverse signaling cascades and numerous compensatory pathways in metastasis, designing broad-spectrum anti-metastatic therapies remains challenging. Although significant anti-cancer activity is evident in specific patients with advanced cancers and metastases treated with single or combination immunotherapies, there are limitations, i.e. toxicity, immune inhibitory 'cold' tumors and the tumor microenvironment (TME), and intra- and intertumoral heterogeneity. Accordingly, multidisciplinary strategies are required to attack metastases and the TME to obtain optimal therapeutic responses.Expert opinion: To create potent anti-metastatic agents, defining critical genes/proteins and drugs controlling discrete steps in the metastatic cascade are mandatory. Melanoma differentiation-associated gene-9 (MDA-9), Syndecan Binding Protein (SDCBP) or Syntenin (MDA-9/Syntenin) is robustly expressed and serves essential roles in cancer disease progression through protein-protein interactions with additional metastasis-associated molecules and pathways. The importance of MDA-9/Syntenin in the metastatic process is now established and first-in-class inhibitory molecules look promising with some moving toward clinical evaluation.","PeriodicalId":12185,"journal":{"name":"Expert Opinion on Therapeutic Targets","volume":" ","pages":"75-92"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12047740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Enhancer of zeste homolog 2 (EZH2) in endocrine tumors: current knowledge and future directions. 内分泌肿瘤中zeste同源物2增强子（EZH2）的研究现状及未来发展方向

IF 4.6 2区医学

Expert Opinion on Therapeutic Targets Pub Date : 2025-03-01 Epub Date: 2025-03-25 DOI: 10.1080/14728222.2025.2482555

Poonam Kumari, Sheenam Garg, Ashutosh Kumar Arya, Jyotdeep Kaur, Naresh Kumar Sachdeva, Uma Nahar Saikia, Divya Dahiya, Sanjay Kumar Bhadada, Sudhaker D Rao

{"title":"Enhancer of zeste homolog 2 (EZH2) in endocrine tumors: current knowledge and future directions.","authors":"Poonam Kumari, Sheenam Garg, Ashutosh Kumar Arya, Jyotdeep Kaur, Naresh Kumar Sachdeva, Uma Nahar Saikia, Divya Dahiya, Sanjay Kumar Bhadada, Sudhaker D Rao","doi":"10.1080/14728222.2025.2482555","DOIUrl":"10.1080/14728222.2025.2482555","url":null,"abstract":"Introduction: Enhancer of zeste homolog 2 (EZH2) is a histone methyltransferase that orchestrates gene expression via epigenetic and non-epigenetic mechanisms. EZH2 performs epigenetic functions by methylating histones and/or non-histone proteins and suppressing or activating target genes. Moreover, non-epigenetic functions involve dysregulation of target genes independent of histone methylation, thereby impacting multiple signaling pathways.Areas covered: EZH2 has emerged as a pivotal player in the initiation of various cancers. EZH2 overexpression facilitated by H3K27me3 is the principal driver. However, the consequent dysregulation of target genes resulting from EZH2 overexpression has emerged as a secondary instigator of tumorigenesis, leading to metastasis and poor prognosis. Further complexity arises from somatic mutations in EZH2 and downstream target genes such as BRAF and RASSF1A. However, understanding its effects on endocrine tumors/cancers remains an underexplored with the potential to significantly enhance clinical outcomes and contribute to human health. Therefore, the present review focuses on the multifaceted functions of EZH2 and its pathophysiological mechanisms in tumor proliferation, with a specific emphasis on endocrine tumors.Expert opinion: Investigating EZH2 mechanisms and targeting with inhibitors and drugs is an active area of research that could offer a promising avenue for treatment and a better understanding of molecular therapeutic interventions.","PeriodicalId":12185,"journal":{"name":"Expert Opinion on Therapeutic Targets","volume":" ","pages":"159-169"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Targeting PCSK9 beyond the liver: evidence from experimental and clinical studies. 靶向肝脏以外的PCSK9：来自实验和临床研究的证据

IF 4.6 2区医学

Expert Opinion on Therapeutic Targets Pub Date : 2025-03-01 Epub Date: 2025-03-30 DOI: 10.1080/14728222.2025.2482545

Lorenzo Da Dalt, Andrea Baragetti, Giuseppe Danilo Norata

{"title":"Targeting PCSK9 beyond the liver: evidence from experimental and clinical studies.","authors":"Lorenzo Da Dalt, Andrea Baragetti, Giuseppe Danilo Norata","doi":"10.1080/14728222.2025.2482545","DOIUrl":"10.1080/14728222.2025.2482545","url":null,"abstract":"Introduction: PCSK9 has been widely studied as a target for lipid-lowering as its inhibition increases LDLR recycling on the surface of hepatocytes, which promotes the catabolism of LDL particles. PCSK9 can be synthesized in extra-hepatic tissues, including in the brain, the pancreas, and the heart, and in immune cells. It is of interest to understand whether the extra-hepatic effects observed when PCSK9 is genetically inhibited by naturally occurring mutations are also recapitulated by pharmacology.Area covered: Genetics studies reported an increased risk of developing new-onset diabetes, ectopic adiposity, and reduced immune-inflammatory responses with PCSK9 deficiency. However, these aspects were not observed in clinical trials and data from real-world medicine with monoclonal antibodies (mAbs) and gene silencing approaches targeting PCSK9.Expert opinion: It is possible that the biological adaptations occurring when PCSK9 is inhibited lifelong, as in the case of genetic studies, could explain the discrepancy with the data obtained by clinical studies testing the pharmacological inhibition of PCSK9. Also, PCSK9 mAbs have been in use for 12 years; thus, probably, in this time window, a pharmacological reduction of circulating PCSK9 up to 80-90% does not lead to changes other than the impressive reduction in LDL-C and in CVD events.","PeriodicalId":12185,"journal":{"name":"Expert Opinion on Therapeutic Targets","volume":" ","pages":"137-157"},"PeriodicalIF":4.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0